**2. Epidemiology, definition, and classification of SLE: an overview**

Systemic lupus erythematosus (SLE) is a nonhomogeneous clinical disorder that has autoimmunity roots. It can be recognized via the presence of autoantibodies produced toward nuclear antigens. According to a classic description, SLE is a multiorgan condition, and affected individuals may show symptoms in highly dissimilar formats. Classification criteria have been established, partly to try to maintain homogeneity within the SLE cases in order to facilitate research efforts. The American College of Rheumatology (ACR) disseminated these criteria that were modified in 1982 [1]. These guidelines integrate clinical presentations with irregularities found in blood exams including a detection of nuclear resistant antibodies or thrombocytopenia. Once again, these criteria were corrected in 1997 to better represent the significance of phospholipid-targeting antibodies in SLE cases [15].

SLE is an insufficiently explained syndrome. Etiology and pathogenesis are not known to date. Still, SLE is a seminal condition that has been a challenge to be resolved for immunologists, biologists, geneticists, and clinicians. The condition can be detected through various, seemingly unrelated presentations. Surprisingly, these symptoms could take place in many stochastically interconnected clusters; despite this, single gene deficits could enhance a narrower range of signs/items often observed in SLE. A lack of internal coherence exists among features (criteria) that contribute to the disease. Such features are considered in the ACR and the systemic lupus collaborating clinics (SLICC) descriptions to categorize SLE. Yet, SLE is a concept because the ACR/SLICC definitions enable scientists to describe hundreds of various SLE subtypes clinically [16].
